ORCID Profile
0000-0003-3922-2914
Current Organisations
University of South Australia
,
University of Sydney
,
Western Sydney Local Health District
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Publisher: Elsevier BV
Date: 10-2011
DOI: 10.1016/J.NIOX.2011.06.005
Abstract: Polycystic ovary syndrome (PCOS) is associated with incremental risk of atherosclerosis and possibly of cardiovascular events. Insulin resistance (IR) occurs frequently in PCOS subjects, which might be one of the mechanisms involved in engendering such risk. We sought to evaluate whether the impact of other factors potentially associated both with PCOS and with IR might differentially modulate degree of IR in women with and without PCOS. We measured body mass index (BMI), hs-CRP, plasma concentrations of asymmetric dimethylarginine (ADMA), vitamin D (25(OH)D3) levels and platelet responsiveness to nitric oxide donor sodium nitroprusside (NO responsiveness) in 47 young women (n=27 with PCOS and n=20 weight-matched controls) without metabolic syndrome, hypertension or overt cardiovascular disease. We performed univariate and multivariate regression analyses to establish correlates of the quantitative insulin-sensitivity check index (QUICKI), as a marker of IR. On univariate analysis, plasma 25(OH)D3 levels and low NO responsiveness tended to be direct correlates with QUICKI in the entire subject group. BMI, hs-CRP, and ADMA levels were significant inverse correlates of QUICKI in PCOS subjects, but not in subjects without PCOS. On multivariate analysis, NO responsiveness, and 25(OH)D3 levels, but not PCOS per se were significant correlates of QUICKI. In the entire cohort of young women, low NO responsiveness and vitamin D deficiency are associated with low QUICKI, while elevated ADMA, inflammatory activation and obesity are selectively associated with low QUICKI in PCOS subjects this may contribute to the increased cardiovascular risk associated with this syndrome.
Publisher: Springer Science and Business Media LLC
Date: 20-07-2017
Publisher: Public Library of Science (PLoS)
Date: 10-05-2017
Publisher: Wiley
Date: 11-02-2015
DOI: 10.1002/EJHF.242
Abstract: The release of the B-type natriuretic peptide (BNP) is increased in heart failure (HF), a condition associated with oxidative stress. BNP is known to exert anti-inflammatory effects including suppression of neutrophil superoxide (O2(-)) release. However, BNP-based restoration of homeostasis in HF is inadequate, and the equivocal clinical benefit of a recombinant BNP, nesiritide, raises the possibility of attenuated response to BNP. We therefore tested the hypothesis that BNP-induced suppression of neutrophil O2(-) generation is impaired in patients with acute HF. We have recently characterized suppression of neutrophil O2(-) generation (PMA- or fMLP-stimulated neutrophil burst) by BNP as a measure of its physiological activity. In the present study, BNP response was compared in neutrophils of healthy subjects (n = 29) and HF patients (n = 45). Effects of BNP on fMLP-induced phosphorylation of the NAD(P)H oxidase subunit p47phox were also evaluated. In acute HF patients, the suppressing effect of BNP (1 µmol/L) on O2(-) generation was attenuated relative to that in healthy subjects (P < 0.05 for both PMA and fMLP). Analogously, BNP inhibited p47phox phosphorylation in healthy subjects but not in HF patients (P < 0.05). However, O2(-)-suppressing effects of the cell-permeable cGMP analogue (8-pCPT-cGMP) were preserved in acute HF. Conventional HF treatment for 5 weeks partially restored neutrophil BNP responsiveness (n = 25, P < 0.05), despite no significant decrease in plasma NT-proBNP levels. BNP inhibits neutrophil O2(-) generation by suppressing NAD(P)H oxidase assembly. This effect is impaired in acute HF patients, with partial recovery during treatment.
Publisher: National Institute for Health and Care Research
Date: 12-2017
DOI: 10.3310/HTA21730
Abstract: Mild frailty or pre-frailty is common and yet is potentially reversible. Preventing progression to worsening frailty may benefit in iduals and lower health/social care costs. However, we know little about effective approaches to preventing frailty progression. (1) To develop an evidence- and theory-based home-based health promotion intervention for older people with mild frailty. (2) To assess feasibility, costs and acceptability of (i) the intervention and (ii) a full-scale clinical effectiveness and cost-effectiveness randomised controlled trial (RCT). Evidence reviews, qualitative studies, intervention development and a feasibility RCT with process evaluation. Two systematic reviews (including systematic searches of 14 databases and registries, 1990–2016 and 1980–2014), a state-of-the-art review (from inception to 2015) and policy review identified effective components for our intervention. We collected data on health priorities and potential intervention components from semistructured interviews and focus groups with older people (aged 65–94 years) ( n = 44), carers ( n = 12) and health/social care professionals ( n = 27). These data, and our evidence reviews, fed into development of the ‘HomeHealth’ intervention in collaboration with older people and multidisciplinary stakeholders. ‘HomeHealth’ comprised 3–6 sessions with a support worker trained in behaviour change techniques, communication skills, exercise, nutrition and mood. Participants addressed self-directed independence and well-being goals, supported through education, skills training, enabling in iduals to overcome barriers, providing feedback, maximising motivation and promoting habit formation. Single-blind RCT, in idually randomised to ‘HomeHealth’ or treatment as usual (TAU). Community settings in London and Hertfordshire, UK. A total of 51 community-dwelling adults aged ≥ 65 years with mild frailty. Feasibility – recruitment, retention, acceptability and intervention costs. Clinical and health economic outcome data at 6 months included functioning, frailty status, well-being, psychological distress, quality of life, capability and NHS and societal service utilisation/costs. We successfully recruited to target, with good 6-month retention (94%). Trial procedures were acceptable with minimal missing data. In idual randomisation was feasible. The intervention was acceptable, with good fidelity and modest delivery costs (£307 per patient). A total of 96% of participants identified at least one goal, which were mostly exercise related (73%). We found significantly better functioning (Barthel Index +1.68 p = 0.004), better grip strength (+6.48 kg p = 0.02), reduced psychological distress (12-item General Health Questionnaire –3.92 p = 0.01) and increased capability-adjusted life-years [+0.017 95% confidence interval (CI) 0.001 to 0.031] at 6 months in the intervention arm than the TAU arm, with no differences in other outcomes. NHS and carer support costs were variable but, overall, were lower in the intervention arm than the TAU arm. The main limitation was difficulty maintaining outcome assessor blinding. Evidence is lacking to inform frailty prevention service design, with no large-scale trials of multidomain interventions. From stakeholder ublic perspectives, new frailty prevention services should be personalised and encompass multiple domains, particularly socialising and mobility, and can be delivered by trained non-specialists. Our multicomponent health promotion intervention was acceptable and delivered at modest cost. Our small study shows promise for improving clinical outcomes, including functioning and independence. A full-scale in idually RCT is feasible. A large, definitive RCT of the HomeHealth service is warranted. This study is registered as PROSPERO CRD42014010370 and Current Controlled Trials ISRCTN11986672. This project was funded by the National Institute for Health Research (NIHR) Health Technology Assessment programme and will be published in full in Health Technology Assessment Vol. 21, No. 73. See the NIHR Journals Library website for further project information.
Publisher: Oxford University Press (OUP)
Date: 02-08-2013
Publisher: Elsevier BV
Date: 11-2016
Location: Sri Lanka
No related grants have been discovered for Anjalee Thanuja Amarasekera.